Beneficial cardiac effects of enalapril in postmenopausal hypertensive rats

ZILBERMAN JUDITH; YANES LICY; TOMAT ANALIA; ROMERO MARIANA; SARTORI-VALLINOTI JULIO; ELESGARAY ROSANA; COSTA MARIA DE LOS ANGELES; RECKELHOFF JANE; ARRANZ CRISTINA

New Orleans, USA

Congreso; Experimental Biology 2009; 2009

American Physiology Society

Several studies suggest an interaction between renin-angiotensin system and estrogen with nitric oxide (NO) system and oxidative stress. Objective: To evaluate the effects of the angiotensin-converting enzyme inhibitor enalapril (E) on systolic blood pressure (SBP), oxidative stress, NO synthase (NOS) activity and estrogen receptors expression in the left ventricle (LV) of postmenopausal spontaneously hypertensive rats (OF-SHR). aged 16 month received E 250 mg/L in drinking water or tap water (C) for 30 days. At the end of the treatment lipid peroxidation end products (TBARS), estrogen receptors expression, catalase (CAT), glutathion peroxidase (GPx) and NOS activity were measured in LV. Results: Treatment with enalapril decreased SBP and lipid peroxidation but increased GPx and NOS activity in OF- SHR. Estrogen receptor ¦Â was upregulated by E treatment in LV of OF-SHR. SBP                          TBARS                         CAT                    GPx                                NOS activity              (mmHg)               (ng/mg.prot)           (pmol/mg.prot)    ( pmol/min.mg.prot)     (pmol.citrulline14C/g tissue. min) C             174¡À10                   0.215¡À0.029           0.062¡À0.006           2.30¡À0.10                               348.1¡À3.8 E             152¡À9#                   0.137¡À0.006*         0.039¡À0.009           2.94¡À0.20*                             445.3¡À13.5* * p<0.02 vs control, #p<0.01 vs control. In conclusi¨®n, our study shows that enalapril administration caused a reduction in oxidative stress and increases in NOS activity and estrogen receptor ¦Â expression in LV of OF-SHR. These results suggest that changes observed in the LV after menopause may be Angiotensin II mediated.